2024/04/25 更新

写真a

ワカスギ　タカユキ
若杉　嵩幸
WAKASUGI Takayuki
所属
医歯学総合病院 魚沼地域医療教育センター 特任助教
職名
特任助教
外部リンク

学位

  • 博士(医学) （ 2019年9月   新潟大学 ）

経歴

  • 新潟大学   医歯学総合病院 魚沼地域医療教育センター   特任助教

    2022年4月 - 現在

 

論文

  • Cardiac mitofusin-1 is reduced in non-responding patients with idiopathic dilated cardiomyopathy. 国際誌

    Yung Ting Hsiao, Ippei Shimizu, Takayuki Wakasugi, Yohko Yoshida, Ryutaro Ikegami, Yuka Hayashi, Masayoshi Suda, Goro Katsuumi, Masaaki Nakao, Takuya Ozawa, Daisuke Izumi, Takeshi Kashimura, Kazuyuki Ozaki, Tomoyoshi Soga, Tohru Minamino

    Scientific reports   11 ( 1 )   6722 - 6722   2021年3月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Prognosis of severe heart failure remains poor. Urgent new therapies are required. Some heart failure patients do not respond to established multidisciplinary treatment and are classified as "non-responders". The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Mitofusin-1 (Mfn1), a mitochondrial fusion protein, is significantly reduced in non-responding patients. This study aimed to elucidate the role of Mfn1 in the failing heart. Twenty-two idiopathic dilated cardiomyopathy (IDCM) patients who underwent endomyocardial biopsy of intraventricular septum were included. Of the 22 patients, 8 were non-responders (left ventricular (LV) ejection fraction (LVEF) of < 10% improvement at late phase follow-up). Electron microscopy (EM), quantitative PCR, and immunofluorescence studies were performed to explore the biological processes and molecules involved in failure to respond. Studies in cardiac specific Mfn1 knockout mice (c-Mfn1 KO), and in vitro studies with neonatal rat ventricular myocytes (NRVMs) were also conducted. A significant reduction in mitochondrial size in cardiomyocytes, and Mfn1, was observed in non-responders. A LV pressure overload with thoracic aortic constriction (TAC) c-Mfn1 KO mouse model was generated. Systolic function was reduced in c-Mfn1 KO mice, while mitochondria alteration in TAC c-Mfn1 KO mice increased. In vitro studies in NRVMs indicated negative regulation of Mfn1 by the β-AR/cAMP/PKA/miR-140-5p pathway resulting in significant reduction in mitochondrial respiration of NRVMs. The level of miR140-5p was increased in cardiac tissues of non-responders. Mfn1 is a biomarker of heart failure in non-responders. Therapies targeting mitochondrial dynamics and homeostasis are next generation therapy for non-responding heart failure patients.

    DOI： 10.1038/s41598-021-86209-y

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  • Increased acetylcarnitine does not mediate cardioprotective effects of empagliflozin in a murine heart failure model(和訳中) 査読

    仲尾 政晃, 清水 逸平, 吉田 陽子, 勝海 悟郎, 林 由香, 池上 龍太郎, 須田 将吉, 若杉 嵩幸, 南野 徹

    日本抗加齢医学会総会プログラム・抄録集   19回   211 - 211   2019年6月

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    記述言語：英語   出版者・発行元：(一社)日本抗加齢医学会  

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  • p53 plays a crucial role in endothelial dysfunction associated with hyperglycemia and ischemia. 査読 国際誌

    Masataka Yokoyama, Ippei Shimizu, Ayako Nagasawa, Yohko Yoshida, Goro Katsuumi, Takayuki Wakasugi, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Yusuke Ota, Sho Okada, Marcus Fruttiger, Yoshio Kobayashi, Masanori Tsuchida, Yoshiaki Kubota, Tohru Minamino

    Journal of molecular and cellular cardiology   129   105 - 117   2019年4月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    p53 is a guardian of the genome that protects against carcinogenesis. There is accumulating evidence that p53 is activated with aging. Such activation has been reported to contribute to various age-associated pathologies, but its role in vascular dysfunction is largely unknown. The aim of this study was to investigate whether activation of endothelial p53 has a pathological effect in relation to endothelial function. We established endothelial p53 loss-of-function and gain-of-function models by breeding endothelial-cell specific Cre mice with floxed Trp53 or floxed Mdm2/Mdm4 mice, respectively. Then we induced diabetes by injection of streptozotocin. In the diabetic state, endothelial p53 expression was markedly up-regulated and endothelium-dependent vasodilatation was significantly impaired. Impairment of vasodilatation was significantly ameliorated in endothelial p53 knockout (EC-p53 KO) mice, and deletion of endothelial p53 also significantly enhanced the induction of angiogenesis by ischemia. Conversely, activation of endothelial p53 by deleting Mdm2/Mdm4 reduced both endothelium-dependent vasodilatation and ischemia-induced angiogenesis. Introduction of p53 into human endothelial cells up-regulated the expression of phosphatase and tensin homolog (PTEN), thereby reducing phospho-eNOS levels. Consistent with these results, the beneficial impact of endothelial p53 deletion on endothelial function was attenuated in EC-p53 KO mice with an eNOS-deficient background. These results show that endothelial p53 negatively regulates endothelium-dependent vasodilatation and ischemia-induced angiogenesis, suggesting that inhibition of endothelial p53 could be a novel therapeutic target in patients with metabolic disorders.

    DOI： 10.1016/j.yjmcc.2019.02.010

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  • Peptide vaccine for semaphorin3E ameliorates systemic glucose intolerance in mice with dietary obesity. 国際誌

    Yohko Yoshida, Ippei Shimizu, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Takayuki Wakasugi, Masaaki Nakao, Hironori Nakagami, Ryuichi Morishita, Tohru Minamino

    Scientific reports   9 ( 1 )   3858 - 3858   2019年3月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    We previously demonstrated that cellular aging signals upregulated a secreted class 3 semaphorin E (Sema3E) and its receptor plexinD1 in the adipose tissue of a murine model of dietary obesity and that Sema3E was a chemoattractant, mediating its biological effects by inducing infiltration of plexinD1-positive inflammatory macrophages into the visceral white adipose tissue. This study was performed to develop a peptide vaccine for Sema3E and test its therapeutic potential in a murine model of dietary obesity. Two antigenic peptides were selected to generate neutralizing antibodies for a vaccine. These peptides were conjugated to keyhole limpet hemocyanin (KLH), and were administered with Freund's adjuvant to obese wild-type male mice. The Sema3E antibody titer was analyzed by ELISA, and the biological effects of the peptides were tested in mice with dietary obesity. Among the two candidate peptides, the Sema3E antibody titer was significantly increased by injection of KLH-conjugated HKEGPEYHWS (Sema3E vaccine). Administration of Sema3E vaccine suppressed the infiltration of plexinD1-positive cells, ameliorated chronic inflammation in visceral white adipose tissue, and improved systemic glucose intolerance in mice with dietary obesity, suggesting that Sema3E vaccine has the potential to become a next generation therapy for obesity and diabetes.

    DOI： 10.1038/s41598-019-40325-y

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  • 新しい老化細胞除去薬と加齢および加齢関連心血管代謝障害(A Novel Senolytic Drug for Aging and Age-related Cardiometabolic Disorders) 査読

    勝海 悟郎, 清水 逸平, 吉田 陽子, 林 由香, 池上 龍太郎, 須田 将吉, 若杉 嵩幸, 仲尾 政晃, 長澤 綾子, 南野 徹

    日本循環器学会学術集会抄録集   83回   PJ126 - 4   2019年3月

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    記述言語：英語   出版者・発行元：(一社)日本循環器学会  

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  • Role of smooth muscle cell p53 in pulmonary arterial hypertension. 国際誌

    Takayuki Wakasugi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Masaaki Nakao, Makoto Hoyano, Takeshi Kashimura, Kazufumi Nakamura, Hiroshi Ito, Takashi Nojiri, Tomoyoshi Soga, Tohru Minamino

    PloS one   14 ( 2 )   e0212889 - 7   2019年

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    記述言語：英語   出版者・発行元：(一社)日本循環器学会  

    Pulmonary arterial hypertension (PAH) is characterized by remodeling and narrowing of the pulmonary arteries, which lead to elevation of right ventricular pressure, heart failure, and death. Proliferation of pulmonary artery smooth muscle cells (PASMCs) is thought to be central to the pathogenesis of PAH, although the underlying mechanisms are still being explored. The protein p53 is involved in cell cycle coordination, DNA repair, apoptosis, and cellular senescence, but its role in pulmonary hypertension (PH) is not fully known. We developed a mouse model of hypoxia-induced pulmonary hypertension (PH) and found significant reduction of p53 expression in the lungs. Our in vitro experiments with metabolomic analyses and the Seahorse XF extracellular flux analyzer indicated that suppression of p53 expression in PASMCs led to upregulation of glycolysis and downregulation of mitochondrial respiration, suggesting a proliferative phenotype resembling that of cancer cells. It was previously shown that systemic genetic depletion of p53 in a murine PH model led to more severe lung manifestations. Lack of information about the role of cell-specific p53 signaling promoted us to investigate it in our mouse PH model with the inducible Cre-loxP system. We generated a mouse model with SMC-specific gain or loss of p53 function by crossing Myh11-Cre/ERT2 mice with floxed Mdm4 mice or floxed Trp53 mice. After these animals were exposed to hypoxia for 4 weeks, we conducted hemodynamic and echocardiographic studies. Surprisingly, the severity of PH was similar in both groups of mice and there were no differences between the genotypes. Our findings in these mice indicate that activation or suppression of p53 signaling in SMCs has a minor role in the pathogenesis of PH and suggest that p53 signaling in other cells (endothelial cells, immune cells, or fibroblasts) may be involved in the progression of this condition.

    DOI： 10.1371/journal.pone.0212889

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  • 新規血管老化関連分子SAGPを標的とした抗老化治療 査読

    須田 将吉, 清水 逸平, 吉田 陽子, 林 由香, 勝海 悟郎, 池上 龍太郎, 若杉 嵩幸, 長澤 綾子, 南野 徹

    日本内分泌学会雑誌   94 ( 4 )   1551 - 1551   2018年12月

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    記述言語：日本語   出版者・発行元：(一社)日本内分泌学会  

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  • Gamma-Aminobutyric Acid Signaling in Brown Adipose Tissue Promotes Systemic Metabolic Derangement in Obesity. 査読 国際誌

    Ryutaro Ikegami, Ippei Shimizu, Takeshi Sato, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Goro Katsuumi, Ji Li, Takayuki Wakasugi, Yasuhiko Minokoshi, Shiki Okamoto, Eiichi Hinoi, Søren Nielsen, Naja Zenius Jespersen, Camilla Scheele, Tomoyoshi Soga, Tohru Minamino

    Cell reports   24 ( 11 )   2827 - 2837   2018年9月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Brown adipose tissue (BAT) is a metabolically active organ that contributes to the maintenance of systemic metabolism. The sympathetic nervous system plays important roles in the homeostasis of BAT and promotes its browning and activation. However, the role of other neurotransmitters in BAT homeostasis remains largely unknown. Our metabolomic analyses reveal that gamma-aminobutyric acid (GABA) levels are increased in the interscapular BAT of mice with dietary obesity. We also found a significant increase in GABA-type B receptor subunit 1 (GABA-BR1) in the cell membranes of brown adipocytes of dietary obese mice. When administered to obese mice, GABA induces BAT dysfunction together with systemic metabolic disorder. Conversely, the genetic inactivation or inhibition of GABA-BR1 leads to the re-browning of BAT under conditions of metabolic stress and ameliorated systemic glucose intolerance. These results indicate that the constitutive activation of GABA/GABA-BR1 signaling in obesity promotes BAT dysfunction and systemic metabolic derangement.

    DOI： 10.1016/j.celrep.2018.08.024

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  • Catecholamine-Induced Senescence of Endothelial Cells and Bone Marrow Cells Promotes Cardiac Dysfunction in Mice.

    Goro Katsuumi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Takayuki Wakasugi, Masaaki Nakao, Tohru Minamino

    International heart journal   59 ( 4 )   837 - 844   2018年7月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Previous studies have suggested that cellular senescence plays a central role in the progression of pathologic changes in the failing heart. It is well known that the sympathetic nervous system is activated in patients with heart failure, and this change is associated with poor clinical outcomes. Sympathetic activation increases the levels of various catecholamines, such as epinephrine and norepinephrine, but the contribution of these catecholamines to cellular senescence associated with heart failure remains to be determined. We found that catecholamine infusion induced senescence of endothelial cells and bone marrow cells, and promoted cardiac dysfunction in mice. In C57BL/6NCr mice, the continuous infusion of isoproterenol-induced cardiac inflammation and cardiac dysfunction. Expression of p53, a master regulator of cellular senescence, was increased in the cardiac tissue and bone marrow cells of these mice. Suppression of cellular senescence by genetic deletion of p53 in endothelial cells or bone marrow cells led to improvement of isoproterenol-induced cardiac dysfunction. In vitro studies showed that adrenergic signaling increased the expression of p53 and adhesion molecules by endothelial cells and macrophages. Our results indicate that catecholamine-induced senescence of endothelial cells and bone marrow cells plays a pivotal role in the progression of heart failure. Suppression of catecholamine-p53 signaling is crucial for inhibition of remodeling in the failing heart.

    DOI： 10.1536/ihj.17-313

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  • Amlodipine Inhibits Vascular Cell Senescence and Protects Against Atherogenesis Through the Mechanism Independent of Calcium Channel Blockade.

    Hiromi Kayamori, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Masayoshi Suda, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Tohru Minamino

    International heart journal   59 ( 3 )   607 - 613   2018年5月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Vascular cells have a finite lifespan and eventually enter irreversible growth arrest called cellular senescence. We have previously suggested that vascular cell senescence contributes to the pathogenesis of human atherosclerosis. Amlodipine is a mixture of two enantiomers, one of which (S- enantiomer) has L-type channel blocking activity, while the other (R+ enantiomer) shows ~1000-fold weaker channel blocking activity than S- enantiomer and has other unknown effects. It has been reported that amlodipine inhibits the progression of atherosclerosis in humans, but the molecular mechanism of this beneficial effect remains unknown. Apolipoprotein E-deficient mice on a high-fat diet were treated with amlodipine, its R+ enantiomer or vehicle for eight weeks. Compared with vehicle treatment, both amlodipine and the R+ enantiomer significantly reduced the number of senescent vascular cells and inhibited plaque formation to a similar extent. Expression of the pro-inflammatory molecule interleukin-1β was markedly upregulated in vehicle-treated mice, but was inhibited to a similar extent by treatment with amlodipine or the R+ enantiomer. Likewise, activation of p53 (a critical inducer of senescence) was markedly suppressed by treatment with amlodipine or the R+ enantiomer. These results suggest that amlodipine inhibits vascular cell senescence and protects against atherogenesis at least partly by a mechanism that is independent of calcium channel blockade.

    DOI： 10.1536/ihj.17-265

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  • Dual Antiplatelet Therapy Guided by CYP2C19 Polymorphisms after Implantation of Second-Generation Drug-Eluting Stents for Management of Acute Coronary Syndrome. 査読

    Takuya Ozawa, Masayoshi Suda, Ryutaro Ikegami, Toshiki Takano, Takayuki Wakasugi, Takao Yanagawa, Komei Tanaka, Kazuyuki Ozaki, Satoru Hirono, Tohru Minamino

    International heart journal   59 ( 1 )   21 - 26   2018年1月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Prasugrel, a novel P2Y12 receptor inhibitor, is administered to patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI), but it can increase the risk of bleeding. The Japanese exhibit weaker responses to clopidogrel than other races because of CYP2C19 polymorphisms; thus, it is unclear whether these patients should continue dual antiplatelet therapy (DAPT) using prasugrel or switch to clopidogrel in the chronic phase. Here we evaluated the clinical outcomes of DAPT guided by CYP2C19 polymorphisms after implantation of second-generation drug-eluting stents (DESs) for ACS management. Patients with ACS receiving PCI via DES from November 2011 to March 2015 were divided into two groups: conventional DAPT with clopidogrel (n = 41) and gene-guided DAPT (n = 24). In the gene-guided DAPT group, all patients with ACS were given DAPT using prasugrel as soon as possible; extensive and intermediate metabolizers receiving PCI for the first time were switched to clopidogrel at least 2 weeks after discharge, and intermediate metabolizers with repeated ACS and poor metabolizers continued on DAPT using prasugrel. Notably, gene-guided DAPT significantly reduced major adverse cardiovascular/cerebrovascular events (MACCEs; 22.0% versus 4.2%, hazard ratio [HR]: 0.15, 95% confidence interval [CI]: 0.01-0.81; P = 0.0247). Hemorrhagic complications were observed in 3.1% of patients receiving conventional DAPT and absent in the gene-guided group. Moreover, multivariate analysis showed that gene-guided DAPT significantly decreased MACCE incidence (HR: 0.15, 95% CI: 0.01-0.81; P = 0.033). Collectively, these data suggest that CYP2C19 polymorphism analysis may improve treatment decisions in patients with ACS receiving DES-PCI.

    DOI： 10.1536/ihj.17-005

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  • Boysenberry polyphenol inhibits endothelial dysfunction and improves vascular health. 国際誌

    Ryo Furuuchi, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Masayoshi Suda, Goro Katsuumi, Takayuki Wakasugi, Masaaki Nakao, Tohru Minamino

    PloS one   13 ( 8 )   e0202051   2018年

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Endothelial cells have an important role in maintaining vascular homeostasis. Age-related disorders (including obesity, diabetes, and hypertension) or aging per se induce endothelial dysfunction that predisposes to the development of atherosclerosis. Polyphenols have been reported to suppress age-related endothelial cell disorders, but their role in vascular function is yet to be determined. We investigated the influence of boysenberry polyphenol on vascular health under metabolic stress in a murine model of dietary obesity. We found that administration of boysenberry polyphenol suppressed production of reactive oxygen species (ROS) and increased production of nitric oxide (NO) in the aorta. It has been reported that p53 induces cellular senescence and has a crucial role in age-related disorders, including heart failure and diabetes. Administration of boysenberry polyphenol significantly reduced the endothelial p53 level in the aorta and ameliorated endothelial cell dysfunction in iliac arteries under metabolic stress. Boysenberry polyphenol also reduced ROS and p53 levels in cultured human umbilical vein endothelial cells (HUVECs), while increasing NO production. Uncoupled endothelial nitric oxide synthase (eNOS monomer) is known to promote ROS production. We found that boysenberry polyphenol reduced eNOS monomer levels both in vivo and in vitro, along with an increase of eNOS dimerization. To investigate the components of boysenberry polyphenol mediating these favorable biological effects, we extracted the anthocyanin fractions. We found that anthocyanins contributed to suppression of ROS and p53, in association with increased NO production and eNOS dimerization. In an ex vivo study, anthocyanins promoted relaxation of iliac arteries from mice with dietary obesity. These findings indicate that boysenberry polyphenol and anthocyanins, a major component of this polyphenol, inhibit endothelial dysfunction and contribute to maintenance of vascular homeostasis.

    DOI： 10.1371/journal.pone.0202051

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  • Gamma-Aminobutyric Acid Signaling in Brown Adipose Tissue Promotes Systemic Metabolic Dysfunction in Obesity 査読

    Ikegami Ryutaro, Shimizu Ippei, Yoshida Yoko, Hayashi Yuka, Suda Masayoshi, Katsuumi Goro, Wakasugi Takayuki, Minamino Tohru

    CIRCULATION   136   2017年11月

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  • Inhibition of dipeptidyl peptidase-4 ameliorates cardiac ischemia and systolic dysfunction by up-regulating the FGF-2/EGR-1 pathway 査読

    Masayoshi Suda, Ippei Shimizu, Yohko Yoshida, Yuka Hayashi, Ryutaro Ikegami, Goro Katsuumi, Takayuki Wakasugi, Yutaka Yoshida, Shujiro Okuda, Tomoyoshi Soga, Tohru Minamino

    PLOS ONE   12 ( 8 )   e0182422   2017年8月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：PUBLIC LIBRARY SCIENCE  

    Dipeptidyl peptidase 4 inhibitors are used worldwide in the management of diabetes, but their role in the prevention or treatment of cardiovascular disorders has yet to be defined. We found that linagliptin, a DPP-4 inhibitor, suppressed capillary rarefaction in the hearts of mice with dietary obesity. Metabolomic analysis performed with capillary electrophoresis/mass spectrometry (LC-MS/MS) showed that linagliptin promoted favorable metabolic remodeling in cardiac tissue, which was characterized by high levels of citrulline and creatine. DNA microarray analysis revealed that the cardiac tissue level of early growth response protein 1 (EGR-1), which activates angiogenesis, was significantly reduced in untreated mice with dietary obesity, while this decrease was inhibited by administration of linagliptin. Mature fibroblast growth factor 2 (FGF-2) has a putative truncation site for DPP-4 at the NH2-terminal, and LC-MS/MS showed that recombinant DPP-4 protein cleaved the NH2-terminal dipeptides of mature FGF-2. Incubation of cultured neonatal rat cardiomyocytes with FGF-2 increased Egr1 expression, while it was suppressed by recombinant DPP-4 protein. Furthermore, vascular endothelial growth factor-A had a critical role in mediating FGF-2/EGR-1 signaling. In conclusion, pharmacological inhibition of DPP-4 suppressed capillary rarefaction and contributed to favorable remodeling of cardiac metabolism in mice with dietary obesity.

    DOI： 10.1371/journal.pone.0182422

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  • A Case of Chronic Lupus Myocarditis 査読

    Takayuki Wakasugi, Hiroaki Obata, Go Hasegawa, Takeshi Kashimura, Haruo Hanawa, Tohru Minamino

    JOURNAL OF CARDIAC FAILURE   19 ( 10 )   S159 - S159   2013年10月

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    記述言語：英語   出版者・発行元：CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS  

    DOI： 10.1016/j.cardfail.2013.08.412

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  • Evolving J waves prior to ventricular fibrillation postoperative coronary bypass.

    Hitoshi Kitazawa, Takayuki Wakasugi, Tsutomu Sugimoto, Kazuo Yamamoto, Shinpei Yoshii, Yoshifusa Aizawa

    Internal medicine (Tokyo, Japan)   50 ( 20 )   2337 - 40   2011年

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    A 74-year-old man without history of ventricular arrhythmias underwent coronary bypass surgery for 3-vessel disease. On the 4th postoperative day, he developed ventricular fibrillation (VF). His monitored ECG showed no elevation of the ST-segment and no prolongation of QT interval, but evolving J waves prior to VF were shown. These J waves gradually decreased after defibrillation. The subsequent angiography revealed patent grafts and normal left ventricular function. J waves reappeared in inferior leads when contrast medium was injected into the coronary artery. Therefore, evolving J wave can be a marker of latent ischemia and a predictor of VF.

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受賞

  • 第250回 日本循環器学会関東甲信越地方会 Clinical Research Award 優秀賞

    2018年12月  

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